Methods of treating and diagnosing parkinsons disease and related dysautonomic disorders

ABSTRACT

A method for treating a Parkinson&#39;s patient with digestive/pancreatic enzymes involves administering an effective amount of digestive/pancreatic enzymes to an individual having the disorder in order to improve a symptom of the disorder. In addition, a method is provided for determining whether an individual has, or may develop, Parkinson&#39;s disease or related dysautonomic disorders and for determining whether an individual will benefit from the administration of pancreatic/digestive enzymes to treat the dysautonomic disorder.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a continuation application of U.S. application Ser.No. 12/046,252, filed on Mar. 11, 2008, which is a divisionalapplication of U.S. application Ser. No. 11/555,697, filed Nov. 2, 2006,which is a continuation-in-part of U.S. application Ser. No. 10/730,567,filed Dec. 8, 2003, which is a continuation of U.S. application Ser. No.09/929,592, filed Aug. 14, 2001, which claims the benefit of U.S.Provisional Application No. 60/224,991, filed Aug. 14, 2000. Each ofthese applications are herein incorporated in their entirety byreference.

FIELD OF THE INVENTION

The present invention generally relates to a method for treatingParkinson's disease and related dysautonomic disorders and a method fordiagnosing individuals with Parkinson's disease or related dysautonomicdisorders. More particularly, the invention relates to a diagnosismethod of analyzing a stool sample of an individual for the presence ofa biological marker (or marker compound) that provides an indication ofwhether the individual has, or can develop, Parkinson's disease or arelated dysautonomic disorder, as well as a therapeutic method fortreating Parkinson's disease or a related dysautonomic disorder by theadministration of pancreatic/digestive enzymes.

BACKGROUND OF THE INVENTION

The nervous system of the body is comprised of two separate systems, thecentral nervous system and the peripheral nervous system. The peripheralnervous system is comprised of the somatic or “voluntary” nervous systemand the autonomic or “automatic” nervous system.

The autonomic nervous system is further broken down into theparasympathetic, sympathetic, and enteric nervous systems. Additionally,it is known that the adrenal glands help to support the sympatheticresponses of the autonomic nervous system and the enteric nervous systemdeals exclusively with the gastrointestinal system. With some overlapthey each control various autonomic functions of the body throughregulation so neurotransmitter releases which affect nervous control

Acetylcholine is a neurotransmitter used by the parasympathetic nervoussystem, while nor epinephrine is utilized by the sympathetic nervoussystem. The adrenal glands secrete epinephrine which help to support thesympathetic nervous system. Norepinephrine and epinephrine together witha substance most affected in Parkinson's disease; dopamine, make up acategory of hormones known as the catecholamines.

The enteric nervous system exerts tremendous control over the digestiveprocesses of the body, including gastrointestinal blood flow, secretionabsorption, and overall breakdown of food. The enteric nervous systemcontains a significant number of neurons, thought to be as numerous asthose found in the central nervous system. The enteric nervous system iscomprised of three types of neurons: sensory, motor, and interneurons.While the sensory neurons are able to determine the environment of thelumen including chemical, ph, thermal and mechanical changes within thelumen, the motor neurons, including those to the pancreatic exocrinecells, control digestion and play a major role in the breakdown of foodand the ultimate absorption of nutrients.

There are two network of nerve plexuses which constitute the entericnervous system: the myenteric plexus and the submucous plexus. The twoplexuses extend from the esophagus to the anus and thus run almost theentire route of the gastrointestinal system.

The submucous plexus, which is not continuous throughout thegastrointestinal tract, is located in the submucosal layer of thegastrointestinal tract. Its primary function is to assess the luminalactivity of the GI system, and therefore exert tremendous control overGI blood flow, secretions into the lumen and absorption rates of suchthings as nutrients, water, and hormones such as secretin which issecreted into the blood stream as a result of the enteric nervoussystems determination of low Ph of the bolus of food entering the smallintestine. This further ultimately determines the role of thepancreatic/digestive enzymes.

The myenteric plexus controls digestive motility and is located inbetween the longitudinal and circular layers of muscle in the tunicamuscularis. It is this segment of the enteric nervous system which maybe initially affected in Parkinson's disease.

The overall digestive process includes the communication between theautonomic (enteric) nervous system and the central nervous system asdigestion does not happen solely as a function of the autonomic nervoussystem. Additionally, there are significant enteric hormones that affectdigestion, including secretin, which are under the control of theautonomic nervous system. From the autonomic nervous system, there is anoverall increase in the stimulation of digestion from theparasympathetic branch of the autonomic nervous system which occursmainly through the secretion of the neurotransmitter acetylcholine,while norepinephrine, secreted by the sympathetic nervous systemdecreases digestion in the gastrointestinal tract.

Dysautonomias are diseases and syndromes that relate to the autonomicnervous system of the individual. Hence in individuals afflicted withdysautonomias, many normal and automatic functions of the body are leftwith poor function or little to no function at all.

There are a plethora of dysautonomic disorders in which the symptoms ofautonomic dysfunction are manifest. For instance, Parkinson's disease ismarked by mild to severe autonomic dysfunction including changes ingait, tremor, discoordination, increased salivary flow, and overall lossof autonomic function. Additionally, changes in executive function aretypically noted in a Parkinson's patient, often allowing the patient toappear as having Alzheimer's disease and resulting in misdiagnosis.Executive function disorders are also found in autistic children.

It has been noted that a lack of secretin response, which is directlyunder the control of the enteric nervous system, may underlie may otherconditions. Further, the use of secretin directly as a therapeutic agentmay be efficacious as in the case of those with familial dysautonomia.

Parkinson's disease is widespread throughout the Western hemisphere andwas first reported by physician James Parkinson in 1817. Parkinson'sdisease is first detected as a tremor in a limb, and ultimatelyprogresses to include 3 manifestations: (i) rigidity, which ischaracterized by “cog-wheel” like movement and “lead-pipe” rigidity;(ii) bradykinesia or slowness in movement, and (iii) posturalinstability associated with a stooped stance and an impaired gait. Thesealtered movements are features of the motor dysfunction, but in additionthere can also be a mental impairment in as many as 40% of allParkinson's patients.

It is known that Parkinson's disease is caused by a deficient state oflevo-dopamine in the brain. More specifically, levo-dopa induceddyskinesis in Parkinson's patients is thought to be a result ofdenervation of the substantia nigra. To date, medical science has notfound a substrate that would allow an injectable form of levo-dopa toreach the brain and successfully cross the blood brain barrier. Thecurrent dopamine replacement therapy is aimed at either directreplacement or mimicking the action at the dopamine receptor sites inthe brain. Sinemet™. and Sinemet CR™ are the two major drugs suited tothat end. While the levo-dopa therapy can create some beneficial changesinitially, those changes generally wane over time, and produce otherproblems such as severe sleep disturbance, dyskinesias, and constantnausea. Medical approaches to Parkinson's disease include surgicaldestruction of the tissue of the brain and the insertion ofmicroelectrodes (deep brain electrical stimulation) to effected portionsof the brain. The insertion of electrodes has the advantage of beingreversible. These interventions, however, are generally transient andneither produces a permanent change in the Parkinsonian state norreverses the effects of the disease.

Some authors suggest that Parkinson's disease is a multifactor,neurodegenerative disorder, which evolves due to excessive oxidation.The substantia nigra is susceptible to oxidative damage which supportsthis theory of the formation of Parkinson's disease. Abnormalities ofthe oxidative phosphorylation impair the mitochondria of the substantianigra, and intensify free radical generation.

While the dyskinesias and loss of executive functioning of the brainreceive the most significant mention with respect to Parkinson'sdisease, other physical manifestations exist that are associated withautonomic dysfunction which are often poorly understood. Some of thesemanifestations include, e.g.: esophageal reflux, diarrhea, and othergastrointestinal dysfunction. In addition, excessive sweating, sleepdisturbances and other symptoms of Parkinson's disease are very similarto those found in familial dysautonomia.

It has long been held that protein restricted diets, timed proteinintake diets, or low protein diets were essential for the absorption ofcertain medications, especially levo-dopa, in the patient afflicted withParkinson's disease. Many studies have demonstrated the possibility thatthe large neutral amino acids (tryptophan, valine, isoleucine, leucine,tyrosine, phenylalanine) may interfere with the absorption of the1-dopamine. Numerous studies have been performed and much postulationhas been made about various diets. It has long been held by the inventorthat there was a decrease in protein digestion in the dysautonomicpatient, including those with Parkinson's disease. This lack of proteindigestion would therefore necessitate an alteration in the proteinintake in individuals with this type of dysfunction, including adecrease in the ingestion of certain proteins which may be difficult todigest without the presence of the necessary digestive enzyme and/orproper functioning of the secretin mechanism, and the over-ingestion ofprotein to make up for that which is not digested when there in anapparent impairment in protein digestive function. For example, if anindividual needed 40 grams of protein a day to sustain function, but hadonly a mechanism which was 10% effective then the individual wouldgravitate toward a diet which was higher in protein and protein whichwould be easier to digest.

This fact has recently been demonstrated in a paper found in MovementDisorders: Protein Intake in Parkinsonian patients using the EPIC foodfrequency questionnaire by Marczewska on Apr. 18, 2006. In this paper,45 Parkinson's patients were evaluated using the EPIC foodquestionnaire. While average caloric intake was normal in theParkinson's patients, they consumed significantly higher amounts ofprotein (mainly in the form of vegetable proteins). The overall proteinintake was 50% higher than the recommended daily allowance (1.2 g/kg vs.0.8 g/kg). More importantly, it showed that the more severe the symptomsof the patient, the greater the protein intake by the patient.

Further, chymotrypsin appears to continue to be a biomarker for thosewith Parkinson's disease as the chymotrypsin cleaves only essentialamino acids. If there is a dearth of chymotrypsin, then the essentialamino acids needed by the body will not be available, and a greateringestion of protein may be needed in order to attain sufficientessential amino acids.

Accordingly, in view of such findings, a method for determining whetheran individual suffering from a dysautonomic disorder and/or any disordercomprising dysautonomic components will benefit from the administrationof secretin, or pancreatic/digestive enzymes, would be highlyadvantageous. In addition, a method for aiding in the diagnosis ofindividuals who may develop Parkinson's disease and related conditionsor symptoms is highly desirable.

SUMMARY OF THE INVENTION

The present invention is directed to methods for aiding in the diagnosisof Parkinson's disease and related disorders, and for treatingindividuals diagnosed as having Parkinson's disease or relateddisorders.

In one embodiment, a method is provided for treating Parkinson's diseasepatients, including those who are likely to develop the disorder orthose who presently have the disorder, through the administration ofdigestive/pancreatic enzymes.

In another embodiment, a diagnostic method is provided for determiningwhether an individual has, or may develop, Parkinson's disease orrelated disorders and for determining whether an individual will benefitfrom the administration of pancreatic/digestive enzymes to treat thedysautonomic disorder. In one embodiment, the diagnostic method analyzesa compound in a stool sample of an individual and correlates theanalysis of the compound with a dysautonomic disorder or condition orthe lack thereof. In one embodiment, the compound to be analyzed is apancreatic enzyme, such as chymotrypsin, or any compound that providesan indication of either protein digestion or metabolism, pancreaticfunction, or an inflammatory process, or a combination thereof. In oneembodiment, the analysis determines a quantitative level of the compoundin the stool.

In a further embodiment, a method for treating a Parkinson's patientwith digestive/pancreatic enzymes involves administering an effectiveamount of digestive/pancreatic enzymes to an individual having thedisorder in order to improve a symptom of the disorder.

In yet another embodiment, a method for treating a Parkinson's patientwith digestive enzymes/pancreatic enzymes involves analyzing a compoundin a stool sample of the individual in which the administration of thedigestive enzymes/pancreatic enzymes is based on the analysis of thestool sample. In one embodiment, the compound to be analyzed comprises apancreatic enzyme, such as chymotrypsin, or any compound that providesan indication of either protein digestion or metabolism, pancreaticfunction, or an inflammatory process, or a combination thereof.

In yet a further embodiment, a process for analyzing the stool sampleinvolves measuring a quantitative level of a pancreatic enzyme, such aschymotrypsin, present in the stool sample and comparing the measuredquantitative level with at least one threshold level to determine theefficacy of the digestive enzyme/pancreatic enzyme administration to theindividual. In one embodiment, the threshold level is based on a levelof the pancreatic enzyme associated with at least one other individualof the same approximate age that does not have Parkinson's disease.

In an additional embodiment, a formulation of digestiveenzymes/pancreatic enzymes is provided which is efficacious for thetreatment of Parkinson's disease and related disorders.

The features and advantages described herein are not all-inclusive and,in particular, many additional features and advantages will be apparentto one of ordinary skill in the art in view of the drawings,specification, and claims. Moreover, it should be noted that thelanguage used in the specification has been principally selected forreadability and instructional purposes, and not to limit the scope ofthe inventive subject matter.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a graph demonstrating the decrease in occurrences ofconstipation in Parkinson's patients after administration of digestiveenzymes over a period of 180 days.

FIG. 2 is a graph demonstrating the increase in the number of bowelmovements in Parkinson's patients after administration of digestiveenzymes over a period of 180 days.

FIG. 3 is a graph demonstrating the decrease in occurrences of tremorsin Parkinson's patients after administration of digestive enzymes over aperiod of 180 days.

FIG. 4 is a graph demonstrating the decrease in occurrences of falls inParkinson's patients after administration of digestive enzymes over aperiod of 180 days.

FIG. 5 is a graph demonstrating the changes in ambulation in Parkinson'spatients after administration of digestive enzymes over a period of 180days.

FIG. 6 is a graph demonstrating the difference in the fecal chymotrypsinlevels of Parkinson's and non-Parkinson's subjects.

DETAILED DESCRIPTION

The present invention is directed to methods for aiding in the diagnosisof dysautonomic disorders and dysautonomic conditions, and for treatingindividuals diagnosed as having a dysautonomic disorder and otherdisorders having dysautonomic components. In one embodiment, a method isprovided for determining the presence of abnormal protein digestionand/or pancreatic dysfunction of an individual, especially a child, byanalyzing a stool sample of the individual for the quantitative levelsof one or more pancreatic enzymes including, but not limited to,chymotrypsin, so as to determine if the individual has, or may develop,a dysautonomic disorder or condition. In another embodiment, a method isprovided for determining whether the individual is likely to benefitfrom the administration of secretin, CCK, VIP, digestive enzymes, otherpeptides, and/or neuropeptides. Until now, there has been no clearbiological marker for dysautonomic disorders or conditions to allowearly diagnosis or screening of such disorders or conditions.

It has been discovered by the inventor herein that a population ofindividuals suffering from dysautonomic disorders such as Parkinson'sdisease have abnormal or pathologic levels of pancreatic enzymes such aschymotrypsin in their stools. It is postulated that in dysautonomicsyndromes, the partial paresis of the gastrointestinal tract, andtherefore the lack of functioning of the secretory cells of the proximalsmall intestine, preclude the proper formation and/or release ofsecretin. It is further postulated that this abnormal protein digestion,as reflected by the low levels of pancreatic enzymes such aschymotrypsin, can be improved by the administration of secretin, CCK,VIP, other neuropeptides, peptides, and/or digestive enzymes to therebyameliorate the symptoms of dysautonomic conditions. Indeed, as a lowmeasure of fecal chymotrypsin, for example, expresses an abnormality ofprotein digestion and/or pancreatic dysfunction, it is postulated thatan improvement of protein digestion to promote normal growth anddevelopment of an individual suffering from a dysautonomic disorder ordysautonomic condition by the administration of secretin, CCK, VIP,other neuropeptides and/or peptides and/or digestive enzymes, canameliorate the dysautonomic symptoms.

In one embodiment, a stable preparation of digestive/pancreatic enzymesis formed into a dosage formulation containing a therapeuticallyeffective amount of a protease, an amylase, and/or a lipase. Theformulation may include additional enzymes, such as pancreatin,chymotrypsin, trypsin, papain and/or papaya. The dosage formulation maybe administered by an oral preparation including, but not limited to, anencapsulated tablet, mini-tabs, microcapsule, mini-capsule, timereleased capsule, sprinkle or other methodology. In one embodiment, theoral preparation is encapsulated using Prosolv technology.Alternatively, the oral preparation may be encapsulated using entericcoating, lipid encapsulation, direct compression, dry granulation, wetgranulation, and/or a combination of these methods.

The dosage formulations may be as follows (USP=U.S. Pharmacopeia):

EXAMPLE 1

Amylase 10,000-70,000 USP units/mg Protease 10,000-80,000 USP units/mgLipase 4,000-40,000 USP units/mg Pancreatin 2,000-6,000 USP units/mgChymotrypsin 2-5 mg Trypsin 60-100 mg Papain 3,000-30,000 USP units/mgPapaya 30-500 mg

EXAMPLE 2

Protease 40,000 USP units/mg Chymotrypsin 2-7 mg Trypsin 60-100 mgPapaya 30-500 mg

EXAMPLE 3

Amylase 30,000 USP units/mg Protease 40,000 USP units/mg Lipase 30,000USP units/mg Chymotrypsin 2-7 mg Papaya 30-500 mg

EXAMPLE 4

Amylase 30,000 USP units/mg Protease 40,000-80,000 USP units/mg Lipase30,000-80,000 USP units/mg Chymotrypsin 2 mg Papain 6,000-30,000 USPunits/mg

Other combinations of digestive enzymes may also be used. These enzymescan be in the form of animal or plant derivatives, natural or synthetic.

In a study conducted by the inventor, sixteen subjects diagnosed withParkinson's disease and ranging in age from 41 to 71 were examined wereexamined. Physical symptoms of the disease, such as constipation, lackof bowel movements, tremors, falling, and an inability to walk weremonitored and measured over a period of 180 days. The subjects weregiven a dosage of digestive enzymes 3-5 per day. The dosages wereadministered in the form of encapsulated tablets, capsules, andsprinkles. The dosages were taken with meals and snacks. The digestiveenzyme dosage included, but was not limited to, one or more of thefollowing: amylases, proteases, pancreatin, papain, papaya, lipases,chymotrypsin, and trypsin.

Ninety-five percent of adults have bowel movements between three and 21times per week, and this would be considered normal. The most commonpattern is one bowel movement a day. However, some people do not havebowel movements every day or the same number of bowel movements eachday. Medically speaking, constipation usually is defined as fewer thanthree bowel movements per week. Severe constipation is defined as lessthan one bowel movement per week.

Referring to FIG. 1, a majority of the subjects experienced moderate tosevere constipation prior to any treatment with digestive enzymes. Theseverity of the constipation was measured on a scale of 1 to 7, with 1equaling no constipation and 7 equaling severe constipation. Thesubjects were monitored at 30, 90, 120 and 180 day intervals. Over thecourse of the 180 day treatment, the severity of the constipationdecreased from severe to moderate to mild in the majority of thesubjects.

Referring to FIG. 2, the number of bowel movements per week experiencedby most of the subjects was lower than normal prior to any treatmentwith digestive enzymes. The subjects were monitored at 30, 90, 120 and180 day intervals. Over the course of the 180 day treatment, the numberof bowel movements per week increased to 3 or more in the majority ofsubjects.

Static tremors, or “resting tremors”, are tremors that occurs despitethe limb being fully supported and at rest against gravity. They usuallyprogress at the rate of 4-7 Hz (hertz), and are the typical Parkinsoniantremor. The amplitude of the tremor often decrease with sleep, completerelaxation or voluntary activity. Tremors are often the first symptomthat people with Parkinson's disease or their family members notice.Initially, the tremors may appear in just one limb (arm or leg) or onlyon one side of the body. The tremors also may affect the lips, tongue,neck, or eyelids. As the disease progresses, the tremors may spread toboth sides of the body, although in some cases the tremors remain onjust one side. Emotional and physical stress tend to make the tremorsworse.

Referring to FIG. 3, a majority of the subjects experienced severetremors prior to any treatment with digestive enzymes. The severity ofthe tremors was measured on a scale of 1 to 7, with 1 equaling notremors and 7 equaling severe tremors. The subjects were monitored at30, 90, 120 and 180 day intervals. Over the course of the 180 daytreatment, the severity of the tremors decreased from severe to moderateto mild in a majority of the subjects.

Many Parkinson's patients develop gait and balance problems and this canlead to falls. Ambulation is with a stooped posture using a short,shuffling gait. This is primarily due to the loss of balance control.Unfortunately with Parkinson's disease, the muscles become stiff andpatients have difficulty swinging their arms when walking which helps inkeeping one's balance. They also have episodes of freezing whichliterally have them “stuck in place” when initiating a step and theyexhibit a slight foot drag which makes tripping easy. Persons withParkinson's have difficulty in judging spatial relationships. Thus,falls often happen when navigating through doorways or through narrowpassages.

Referring to FIG. 4, a majority of the subjects experienced an elevatednumber of falls prior to any treatment with digestive enzymes. Thesubjects were monitored at 30, 90, 120 and 180 days. Over the course ofthe 180 day treatment, the number of falls decreased to less than twoper week in a majority of the subjects.

Referring to FIG. 5, a majority of the subjects experienced severedifficulty in ambulation prior to any treatment with digestive enzymes.The difficulty in ambulation was measured on a scale of 1 to 7, with 1equaling no difficulty and 7 equaling severe difficulty. The subjectswere monitored at 30, 90, 120 and 180 day intervals. Over the course ofthe 180 day treatment, the difficulty in ambulation decreased fromsevere to moderate to some or no difficulty in a majority of thesubjects.

Fecal chymotrypsin levels were also measured in the 16 subjects andcompared to the fecal chymotrypsin levels of 16 subjects who did nothave Parkinson's disease. The non-Parkinson's subjects ranged in agefrom 44 to 77. Fecal chymotrypsin is a sensitive, specific measure ofproteolytic activity. Normal levels of chymotrypsin are considered begreater than 8.4 U/gram. Decreased values (less than 4.2 U/gram) suggestdiminished pancreatic output (pancreatic insufficiency), hypoacidity ofthe stomach or cystic fibrosis. Elevated chymotrypsin values suggestrapid transit time, or less likely, a large output of chymotrypsin fromthe pancreas.

A stool sample was collected from each of the subjects. Each stoolsample was analyzed using an enzymatic photospectrometry analysis todetermine the level of fecal chymotrypsin in the stool. Alternatively,other methods, such as the calorimetric method, use of substrates, useof assays, and/or any other suitable method may be used to measure thefecal chymotrypsin levels. The levels of fecal chymotrypsin in theParkinson's patients was compared to the levels of fecal chymotrypsin inthe non-Parkinson's subjects to determine if the Parkinson's patientswould benefit from the administration of digestive enzymes.

Referring to FIG. 6, the fecal chymotrypsin levels of the Parkinson'spatients ranged from 0.8 to 6.6U/gram, with a mean of 2.84 U/gram, whilethe fecal chymotrypsin levels of the non-Parkinson's patients rangedfrom 9.2. to 47.4 U/gram, with a mean of 28 U/gram. Thus, it can be seenthat the fecal chymotrypsin levels of the Parkinson's patients weremarkedly decreased when compared to the non-Parkinson's subjects.

In summary, the results of the study described herein demonstrate thatadministration of digestive enzymes benefits individuals having adysautonomic disorder, such as Parkinson's disease, by ameliorating thesymptoms of the disorder. Furthermore, the results of the study indicatethat measurement of the fecal chymotrypsin level in individuals having adysautonomic disorder can determine if the individual will benefit fromthe administration of digestive enzymes.

The foregoing description of the embodiments of the invention has beenpresented for the purposes of illustration and description. It is notintended to be exhaustive or to limit the invention to the precise formdisclosed. Many modifications and variations are possible in light ofthis disclosure. It is intended that the scope of the invention belimited not by this detailed description, but rather by the claimsappended hereto.

1. A method of diagnosing a patient comprising: a. obtaining a fecalsample from the patient; b. determining a level of chymotrypsin presentin the fecal sample; and c. diagnosing the patient as having adysautonomic disorder or having a propensity to develop a dysautonomicdisorder if the determined fecal chymotrypsin level is 8.4 U/gram orless.
 2. The method of claim 1, wherein the dysautonomic disorder isselected from a central autonomic disorder, an autonomic neuropathy, adysautonomic syndrome and disorder of the catecholamine family, adisorder of dopamine metabolism, and a dysautonomic syndrome anddisorder of the cardiovascular system.
 3. The method of claim 1, whereinthe dysautonomic disorder is selected from FD, GBS, Parkinson's disease,FFI, diabetic cardiovascular neuropathy, HSAN III, Shy-Drager syndrome,mitral valve prolapse, POTS, idiopathic hypovolemia, Chaga's disease,diabetic autonomic failure, pure autonomic failure, syncope, neurallymediated syncope, hypertension, and SIDS.
 4. The method of claim 1,wherein the dysautonomic disorder is selected from baroreflex failure,dopamine-B-hydroxylase deficiency, pheochromocytoma, chemodectoma,neuroblastoma, familial paranganglioma syndrome, tetrahydrobiopterindeficiency, aromatic-L-amino acid decarboxylase deficiency, Menke'sdisease, orthostatic intolerance, and monoamine oxidase deficiencystates.
 5. The method of claim 1, wherein the fecal chymotrypsin levelis between 8.4 and 4.2 U/gram.
 6. The method of claim 1, wherein thefecal chymotrypsin level is less than 4.2 U/gram.
 7. The method of claim1, wherein the dysautonomic disorder is Parkinson's.
 8. The method ofclaim 1, wherein the dysautonomic disorder is FD.
 9. The method of claim1, wherein the dysautonomic disorder is GBS.
 10. The method of claim 1,wherein the dysautonomic disorder is FFI.
 11. The method of claim 1,wherein the dysautonomic disorder is POTS.
 12. The method of claim 1,wherein the dysautonomic disorder is HSAN III.
 13. The method of claim1, wherein the dysautonomic disorder is Chaga's disease.
 14. The methodof claim 1, wherein the dysautonomic disorder is SIDS.
 15. The method ofclaim 1, wherein the level of chymotrypsin present in the fecal sampleis determined using an enzymatic photospectrometry method.
 16. Themethod of claim 1, further comprising determining if the patientexhibits one or more symptoms of a dysautonomic disorder.
 17. The methodof claim 1, wherein the patient exhibits one or more symptoms of adysautonomic disorder.
 18. The method of claim 1, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 19.The method of claim 18, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 20. The method of claim 18, further comprisingdetermining if the administration of the two or more doses of thepharmaceutical composition reduces one or more symptoms of thedysautonomic disorder.
 21. The method of claim 20, wherein thedetermination comprises a post-administration measurement of one or moresymptoms of the patient.
 22. The method of claim 21, further comprisingcomparing the post-administration measurement of one or more symptoms toa pre-administration measurement of the one or more symptoms.
 23. Amethod of diagnosing a patient comprising: a. determining the level ofchymotrypsin present in a fecal sample obtained from the patient; and b.diagnosing the patient as having a dysautonomic disorder or having apropensity to develop a dysautonomic disorder if the determinedchymotrypsin level is 8.4 U/gram or less.
 24. The method of claim 23,wherein the dysautonomic disorder is selected from a central autonomicdisorder, an autonomic neuropathy, a dysautonomic syndrome and disorderof the catecholamine family, a disorder of dopamine metabolism, and adysautonomic syndrome and disorder of the cardiovascular system.
 25. Themethod of claim 23, wherein the dysautonomic disorder is selected fromFD, GBS, Parkinson's disease, FFI, diabetic cardiovascular neuropathy,HSAN III, Shy-Drager syndrome, mitral valve prolapse, POTS, idiopathichypovolemia, Chaga's disease, diabetic autonomic failure, pure autonomicfailure, syncope, neurally mediated syncope, hypertension, and SIDS. 26.The method of claim 23, wherein the dysautonomic disorder is selectedfrom baroreflex failure, dopamine-B-hydroxylase deficiency,pheochromocytoma, chemodectoma, neuroblastoma, familial parangangliomasyndrome, tetrahydrobiopterin deficiency, aromatic-L-amino aciddecarboxylase deficiency, Menke's disease, orthostatic intolerance, andmonoamine oxidase deficiency states.
 27. The method of claim 23, whereinthe level of chymotrypsin present in the fecal sample is determinedusing an enzymatic photospectrometry method.
 28. The method of claim 23,further comprising determining if the patient exhibits one or moresymptoms of a dysautonomic disorder.
 29. The method of claim 23, furthercomprising administering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 30.The method of claim 29, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 31. A method of confirming a diagnosis of apatient as having a dysautonomic disorder or a propensity to develop adysautonomic disorder, comprising: a. obtaining a fecal sample from thepatient; b. determining a level of chymotrypsin present in the fecalsample; and c. confirming the diagnosis of the patient as having adysautonomic disorder or a propensity to develop a dysautonomic disorderif the determined fecal chymotrypsin level is 8.4 U/gram or less. 32.The method of claim 31, wherein the dysautonomic disorder is selectedfrom a central autonomic disorder, an autonomic neuropathy, adysautonomic syndrome and disorder of the catecholamine family, adisorder of dopamine metabolism, and a dysautonomic syndrome anddisorder of the cardiovascular system.
 33. The method of claim 31,wherein the dysautonomic disorder is selected from FD, GBS, Parkinson'sdisease, FFI, diabetic cardiovascular neuropathy, HSAN III, Shy-Dragersyndrome, mitral valve prolapse, POTS, idiopathic hypovolemia, Chaga'sdisease, diabetic autonomic failure, pure autonomic failure, syncope,neurally mediated syncope, hypertension, and SIDS.
 34. The method ofclaim 31, wherein the dysautonomic disorder is selected from baroreflexfailure, dopamine-B-hydroxylase deficiency, pheochromocytoma,chemodectoma, neuroblastoma, familial paranganglioma syndrome,tetrahydrobiopterin deficiency, aromatic-L-amino acid decarboxylasedeficiency, Menke's disease, orthostatic intolerance, and monoamineoxidase deficiency states.
 35. The method of claim 31, wherein the levelof chymotrypsin present in the fecal sample is determined using anenzymatic photospectrometry method.
 36. The method of claim 31, furthercomprising determining if the patient exhibits one or more symptoms of adysautonomic disorder.
 37. The method of claim 31, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 38.The method of claim 37, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 39. A method of confirming a diagnosis of apatient as having a dysautonomic disorder or a propensity to develop adysautonomic disorder comprising: a. determining the level ofchymotrypsin present in a fecal sample obtained from the patient; and b.confirming the diagnosis of the patient as having a dysautonomicdisorder or a propensity to develop a dysautonomic disorder if thedetermined chymotrypsin level is 8.4 U/gram or less.
 40. The method ofclaim 39, wherein the dysautonomic disorder is selected from a centralautonomic disorder, an autonomic neuropathy, a dysautonomic syndrome anddisorder of the catecholamine family, a disorder of dopamine metabolism,and a dysautonomic syndrome and disorder of the cardiovascular system.41. The method of claim 39, wherein the dysautonomic disorder isselected from FD, GBS, Parkinson's disease, FFI, diabetic cardiovascularneuropathy, HSAN III, Shy-Drager syndrome, mitral valve prolapse, POTS,idiopathic hypovolemia, Chaga's disease, diabetic autonomic failure,pure autonomic failure, syncope, neurally mediated syncope,hypertension, and SIDS.
 42. The method of claim 39, wherein thedysautonomic disorder is selected from baroreflex failure,dopamine-B-hydroxylase deficiency, pheochromocytoma, chemodectoma,neuroblastoma, familial paranganglioma syndrome, tetrahydrobiopterindeficiency, aromatic-L-amino acid decarboxylase deficiency, Menke'sdisease, orthostatic intolerance, and monoamine oxidase deficiencystates.
 43. The method of claim 39, wherein the level of chymotrypsinpresent in the fecal sample is determined using an enzymaticphotospectrometry method.
 44. The method of claim 39, further comprisingdetermining if the patient exhibits one or more symptoms of adysautonomic disorder.
 45. The method of claim 39, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 46.The method of claim 45, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 47. A method of identifying a patient likely tobenefit from administration of a pharmaceutical composition comprisingone or more digestive enzymes comprising: a. obtaining a fecal samplefrom the patient; b. determining a level of chymotrypsin present in thefecal sample; and c. identifying the patient as likely to benefit fromadministration of the pharmaceutical composition if the determined fecalchymotrypsin level is 8.4 U/gram or less and if the patient is diagnosedwith a dysautonomic disorder or a propensity to develop a dysautonomicdisorder.
 48. The method of claim 47, further comprising determining ifthe patient exhibits one or more symptoms of a dysautonomic disorder.49. The method of claim 47, wherein the benefit comprises a reduction inone or more symptoms associated with a dysautonomic disorder.
 50. Themethod of claim 47, wherein the dysautonomic disorder is selected from acentral autonomic disorder, an autonomic neuropathy, a dysautonomicsyndrome and disorder of the catecholamine family, a disorder ofdopamine metabolism, and a dysautonomic syndrome and disorder of thecardiovascular system.
 51. The method of claim 47, wherein thedysautonomic disorder is selected from FD, GBS, Parkinson's disease,FFI, diabetic cardiovascular neuropathy, HSAN III, Shy-Drager syndrome,mitral valve prolapse, POTS, idiopathic hypovolemia, Chaga's disease,diabetic autonomic failure, pure autonomic failure, syncope, neurallymediated syncope, hypertension, and SIDS.
 52. The method of claim 47,wherein the dysautonomic disorder is selected from baroreflex failure,dopamine-B-hydroxylase deficiency, pheochromocytoma, chemodectoma,neuroblastoma, familial paranganglioma syndrome, tetrahydrobiopterindeficiency, aromatic-L-amino acid decarboxylase deficiency, Menke'sdisease, orthostatic intolerance, and monoamine oxidase deficiencystates.
 53. The method of claim 47, wherein the level of chymotrypsinpresent in the fecal sample is determined using an enzymaticphotospectrometry method.
 54. The method of claim 47, further comprisingadministering two or more doses of an effective amount of thepharmaceutical composition comprising one or more digestive enzymes. 55.The method of claim 54, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 56. A method of identifying a patient likely tobenefit from administration of a pharmaceutical composition comprisingone or more digestive enzymes comprising: a. determining the level ofchymotrypsin present in a fecal sample obtained from the patient; and b.identifying the patient as likely to benefit from administration of thepharmaceutical composition if the determined chymotrypsin level is 8.4U/gram or less and if the patient is diagnosed with a dysautonomicdisorder or a propensity to develop a dysautonomic disorder.
 57. Themethod of claim 56, further comprising determining if the patientexhibits one or more symptoms of a dysautonomic disorder.
 58. The methodof claim 56, wherein the benefit comprises a reduction in one or moresymptoms associated with a dysautonomic disorder.
 59. The method ofclaim 56, wherein the dysautonomic disorder is selected from a centralautonomic disorder, an autonomic neuropathy, a dysautonomic syndrome anddisorder of the catecholamine family, a disorder of dopamine metabolism,and a dysautonomic syndrome and disorder of the cardiovascular system.60. The method of claim 56, wherein the dysautonomic disorder isselected from FD, GBS, Parkinson's disease, FFI, diabetic cardiovascularneuropathy, HSAN III, Shy-Drager syndrome, mitral valve prolapse, POTS,idiopathic hypovolemia, Chaga's disease, diabetic autonomic failure,pure autonomic failure, syncope, neurally mediated syncope,hypertension, and SIDS.
 61. The method of claim 56, wherein thedysautonomic disorder is selected from baroreflex failure,dopamine-B-hydroxylase deficiency, pheochromocytoma, chemodectoma,neuroblastoma, familial paranganglioma syndrome, tetrahydrobiopterindeficiency, aromatic-L-amino acid decarboxylase deficiency, Menke'sdisease, orthostatic intolerance, and monoamine oxidase deficiencystates.
 62. The method of claim 56, wherein the level of chymotrypsinpresent in the fecal sample is determined using an enzymaticphotospectrometry method.
 63. The method of claim 56, further comprisingadministering two or more doses of an effective amount of thepharmaceutical composition comprising one or more digestive enzymes. 64.The method of claim 63, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 65. A method of diagnosing a patientcomprising: a. obtaining a fecal sample from the patient; b. determiningif the patient suffers from abnormal protein digestion from an analysisof the fecal sample; and c. diagnosing the patient as having adysautonomic disorder or a propensity to develop a dysautonomic disorderif the patient suffers from abnormal protein digestion and exhibits oneor more symptoms of a dysautonomic disorder.
 66. The method of claim 65,wherein the analysis of the fecal sample is a determination of the fecalchymotrypsin level.
 67. The method of claim 65, wherein the dysautonomicdisorder is selected from a central autonomic disorder, an autonomicneuropathy, a dysautonomic syndrome and disorder of the catecholaminefamily, a disorder of dopamine metabolism, and a dysautonomic syndromeand disorder of the cardiovascular system.
 68. The method of claim 65,wherein the dysautonomic disorder is selected from FD, GBS, Parkinson'sdisease, FFI, diabetic cardiovascular neuropathy, HSAN III, Shy-Dragersyndrome, mitral valve prolapse, POTS, idiopathic hypovolemia, Chaga'sdisease, diabetic autonomic failure, pure autonomic failure, syncope,neurally mediated syncope, hypertension, and SIDS.
 69. The method ofclaim 65, wherein the dysautonomic disorder is selected from baroreflexfailure, dopamine-B-hydroxylase deficiency, pheochromocytoma,chemodectoma, neuroblastoma, familial paranganglioma syndrome,tetrahydrobiopterin deficiency, aromatic-L-amino acid decarboxylasedeficiency, Menke's disease, orthostatic intolerance, and monoamineoxidase deficiency states.
 70. The method of claim 66, wherein the levelof chymotrypsin present in the fecal sample is determined using anenzymatic photospectrometry method.
 71. The method of claim 65, furthercomprising determining if the patient exhibits one or more symptoms of adysautonomic disorder.
 72. The method of claim 65, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 73.The method of claim 72, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 74. A method of diagnosing a patientcomprising: a. determining if the patient suffers from abnormal proteindigestion from an analysis of a fecal sample obtained from the patient;and b. diagnosing the patient as having a dysautonomic disorder or apropensity to develop a dysautonomic disorder if the patient suffersfrom abnormal protein digestion and exhibits one or more symptoms of adysautonomic disorder.
 75. The method of claim 74, wherein thedysautonomic disorder is selected from a central autonomic disorder, anautonomic neuropathy, a dysautonomic syndrome and disorder of thecatecholamine family, a disorder of dopamine metabolism, and adysautonomic syndrome and disorder of the cardiovascular system.
 76. Themethod of claim 74, wherein the dysautonomic disorder is selected fromFD, GBS, Parkinson's disease, FFI, diabetic cardiovascular neuropathy,HSAN III, Shy-Drager syndrome, mitral valve prolapse, POTS, idiopathichypovolemia, Chaga's disease, diabetic autonomic failure, pure autonomicfailure, syncope, neurally mediated syncope, hypertension, and SIDS. 77.The method of claim 74, wherein the dysautonomic disorder is selectedfrom baroreflex failure, dopamine-B-hydroxylase deficiency,pheochromocytoma, chemodectoma, neuroblastoma, familial parangangliomasyndrome, tetrahydrobiopterin deficiency, aromatic-L-amino aciddecarboxylase deficiency, Menke's disease, orthostatic intolerance, andmonoamine oxidase deficiency states.
 78. The method of claim 74, whereinthe analysis of the fecal sample is a determination of the fecalchymotrypsin level.
 79. The method of claim 78, wherein the level ofchymotrypsin present in the fecal sample is determined using anenzymatic photospectrometry method.
 80. The method of claim 74, furthercomprising determining if the patient exhibits one or more symptoms of adysautonomic disorder.
 81. The method of claim 74, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 82.The method of claim 81, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 83. A method of evaluating the efficacy oftreatment of a patient diagnosed with a dysautonomic disorder or apropensity to develop a dysautonomic disorder with a pharmaceuticalcomposition comprising one or more digestive enzymes comprising: a.comparing a pre-treatment fecal chymotrypsin level of the patient withone or more post-treatment fecal chymotrypsin levels of the patient; andb. determining that the treatment is efficacious if the one or morepost-treatment fecal chymotrypsin levels are higher than thepretreatment fecal chymotrypsin level.
 84. The method of claim 83,wherein one or more post-treatment fecal chymotrypsin levels are greaterthan 8.4 U/gram.
 85. The method of claim 83, further comprisingdetermining if one or more symptoms of the dysautonomic disorder in thepatient are reduced at one or more times post-treatment.
 86. The methodof claim 83, wherein the dysautonomic disorder is selected from acentral autonomic disorder, an autonomic neuropathy, a dysautonomicsyndrome and disorder of the catecholamine family, a disorder ofdopamine metabolism, and a dysautonomic syndrome and disorder of thecardiovascular system.
 87. The method of claim 83, wherein thedysautonomic disorder is selected from FD, GBS, Parkinson's disease,FFI, diabetic cardiovascular neuropathy, HSAN III, Shy-Drager syndrome,mitral valve prolapse, POTS, idiopathic hypovolemia, Chaga's disease,diabetic autonomic failure, pure autonomic failure, syncope, neurallymediated syncope, hypertension, and SIDS.
 88. The method of claim 83,wherein the dysautonomic disorder is selected from baroreflex failure,dopamine-B-hydroxylase deficiency, pheochromocytoma, chemodectoma,neuroblastoma, familial paranganglioma syndrome, tetrahydrobiopterindeficiency, aromatic-L-amino acid decarboxylase deficiency, Menke'sdisease, orthostatic intolerance, and monoamine oxidase deficiencystates.
 89. The method of claim 84, wherein the level of chymotrypsinpresent in the fecal sample is determined using an enzymaticphotospectrometry method.
 90. The method of claim 83, further comprisingdetermining if the patient exhibits one or more symptoms of adysautonomic disorder.
 91. A method of determining if an individual hasa propensity to develop a dysautonomic disorder comprising: a.determining the fecal chymotrypsin levels of the patient over a periodof time; and b. determining that the individual has a propensity todevelop a dysautonomic disorder if the determined fecal chymotrypsinlevels exhibit a decreasing trend over time and at least one level is8.4 U/gram or less.
 92. The method of claim 91, wherein the dysautonomicdisorder is selected from a central autonomic disorder, an autonomicneuropathy, a dysautonomic syndrome and disorder of the catecholaminefamily, a disorder of dopamine metabolism, and a dysautonomic syndromeand disorder of the cardiovascular system.
 93. The method of claim 91,wherein the dysautonomic disorder is selected from FD, GBS, Parkinson'sdisease, FFI, diabetic cardiovascular neuropathy, HSAN III, Shy-Dragersyndrome, mitral valve prolapse, POTS, idiopathic hypovolemia, Chaga'sdisease, diabetic autonomic failure, pure autonomic failure, syncope,neurally mediated syncope, hypertension, and SIDS.
 94. The method ofclaim 91, wherein the dysautonomic disorder is selected from baroreflexfailure, dopamine-B-hydroxylase deficiency, pheochromocytoma,chemodectoma, neuroblastoma, familial paranganglioma syndrome,tetrahydrobiopterin deficiency, aromatic-L-amino acid decarboxylasedeficiency, Menke's disease, orthostatic intolerance, and monoamineoxidase deficiency states.
 95. The method of claim 91, wherein the levelof chymotrypsin present in the fecal sample is determined using anenzymatic photospectrometry method.
 96. The method of claim 91, furthercomprising determining if the patient exhibits one or more symptoms of adysautonomic disorder.
 97. The method of claim 91, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes. 98.The method of claim 97, wherein the digestive enzymes comprise one ormore pancreatic enzymes.
 99. The method of claim 1, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C. 100.The method of claim 23, wherein the level of chymotrypsin present in thefecal sample is determined at 30° C.
 101. The method of claim 31,wherein the level of chymotrypsin present in the fecal sample isdetermined at 30° C.
 102. The method of claim 39, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C. 103.The method of claim 47, wherein the level of chymotrypsin present in thefecal sample is determined at 30° C.
 104. The method of claim 56,wherein the level of chymotrypsin present in the fecal sample isdetermined at 30° C.
 105. The method of claim 66, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C. 106.The method of claim 78, wherein the level of chymotrypsin present in thefecal sample is determined at 30° C.
 107. The method of claim 84,wherein the level of chymotrypsin present in the fecal sample isdetermined at 30° C.
 108. The method of claim 91, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C.
 109. Amethod of diagnosing a patient comprising: a. determining a level ofchymotrypsin present in a fecal sample obtained from the patient; and b.diagnosing the patient as having a dysautonomic disorder or having apropensity to develop a dysautonomic disorder if the determined fecalchymotrypsin level is less than a normal fecal chymotrypsin level. 110.The method of claim 109, wherein the level of chymotrypsin present inthe fecal sample is determined at 30° C.
 111. The method of claim 109,wherein the normal fecal chymotrypsin level is a level of fecalchymotrypsin associated with at least one other individual of the sameapproximate age that does not have the disorder.
 112. The method ofclaim 109, further comprising determining if the patient exhibits one ormore symptoms of a dysautonomic disorder.
 113. The method of claim 109,further comprising administering two or more doses of an effectiveamount of a pharmaceutical composition comprising one or more digestiveenzymes.
 114. A method of diagnosing a patient comprising: a.determining a level of chymotrypsin present in a fecal sample obtainedfrom the patient; and b. diagnosing the patient as having a dysautonomicdisorder or having a propensity to develop a dysautonomic disorder ifthe determined fecal chymotrypsin level is less than a threshold fecalchymotrypsin level.
 115. The method of claim 114, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C. 116.The method of claim 114, further comprising determining if the patientexhibits one or more symptoms of a dysautonomic disorder.
 117. Themethod of claim 114, further comprising administering two or more dosesof an effective amount of a pharmaceutical composition comprising one ormore digestive enzymes.
 118. A method of confirming a diagnosis of apatient as having a dysautonomic disorder or having a propensity todevelop a dysautonomic disorder, comprising: a. determining a level ofchymotrypsin present in a fecal sample obtained from the patient; and b.confirming the diagnosis of the patient as having a dysautonomicdisorder or having a propensity to develop a dysautonomic disorder ifthe determined fecal chymotrypsin level is less than a normal fecalchymotrypsin level.
 119. The method of claim 118, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C. 120.The method of claim 118, wherein the normal fecal chymotrypsin level isa level of fecal chymotrypsin associated with at least one otherindividual of the same approximate age that does not have the disorder.121. The method of claim 118, further comprising determining if thepatient exhibits one or more symptoms of a dysautonomic disorder. 122.The method of claim 118, further comprising administering two or moredoses of an effective amount of a pharmaceutical composition comprisingone or more digestive enzymes.
 123. A method of confirming a diagnosisof a patient as having a dysautonomic disorder or having a propensity todevelop a dysautonomic disorder, comprising: a. determining a level ofchymotrypsin present in a fecal sample obtained from the patient; and b.confirming the diagnosis of the patient as having a dysautonomicdisorder or having a propensity to develop a dysautonomic disorder ifthe determined fecal chymotrypsin level is less than a threshold fecalchymotrypsin level.
 124. The method of claim 123, wherein the level ofchymotrypsin present in the fecal sample is determined at 30° C. 125.The method of claim 123, further comprising determining if the patientexhibits one or more symptoms of a dysautonomic disorder.
 126. Themethod of claim 123, further comprising administering two or more dosesof an effective amount of a pharmaceutical composition comprising one ormore digestive enzymes.
 127. A method of identifying a patient likely tobenefit from administration of a pharmaceutical composition comprisingone or more digestive enzymes comprising: a. determining a level ofchymotrypsin present in a fecal sample obtained from the patient; and b.identifying the patient as likely to benefit from administration of thepharmaceutical composition if the determined fecal chymotrypsin level isless than a normal fecal chymotrypsin level and if the patient isdiagnosed with a dysautonomic disorder or a propensity to develop adysautonomic disorder.
 128. The method of claim 127, wherein the levelof chymotrypsin present in the fecal sample is determined at 30° C. 129.The method of claim 127, wherein the normal fecal chymotrypsin level isa level of fecal chymotrypsin associated with at least one otherindividual of the same approximate age that does not have the disorder.130. The method of claim 127, further comprising determining if thepatient exhibits one or more symptoms of a dysautonomic disorder. 131.The method of claim 127, further comprising administering two or moredoses of an effective amount of a pharmaceutical composition comprisingone or more digestive enzymes.
 132. A method of identifying a patientlikely to benefit from administration of a pharmaceutical compositioncomprising one or more digestive enzymes comprising: a. determining alevel of chymotrypsin present in a fecal sample obtained from thepatient; and b. identifying the patient as likely to benefit fromadministration of the pharmaceutical composition if the determined fecalchymotrypsin level is less than a threshold fecal chymotrypsin level andif the patient is diagnosed with a dysautonomic disorder or a propensityto develop a dysautonomic disorder.
 133. The method of claim 132,wherein the level of chymotrypsin present in the fecal sample isdetermined at 30° C.
 134. The method of claim 132, further comprisingdetermining if the patient exhibits one or more symptoms of adysautonomic disorder.
 135. The method of claim 132, further comprisingadministering two or more doses of an effective amount of apharmaceutical composition comprising one or more digestive enzymes.